Protection against influenza infection requires early recognition by inflammatory dendritic cells through C-type lectin receptor SIGN-R1

被引:0
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作者
Miguel Palomino-Segura
Laurent Perez
Yagmur Farsakoglu
Tommaso Virgilio
Irene Latino
Rocco D’Antuono
Nikolaos Chatziandreou
Diego U. Pizzagalli
Guojun Wang
Adolfo García-Sastre
Federica Sallusto
Michael C. Carroll
Olivier Neyrolles
Santiago F. Gonzalez
机构
[1] Università della Svizzera italiana,Institute for Research in Biomedicine
[2] University of Bern,Graduate School of Cellular and Molecular Sciences, Faculty of Medicine
[3] Light Microscopy STP,Institute of Computational Science
[4] The Francis Crick Institute,Department of Microbiology
[5] Università della Svizzera italiana,Global Health and Emerging Pathogen Institute
[6] Icahn School of Medicine at Mount Sinai,Department of Medicine, Division of Infectious Diseases
[7] Icahn School of Medicine at Mount Sinai,Institute for Microbiology
[8] Icahn School of Medicine at Mount Sinai,Program in Cellular and Molecular Medicine
[9] ETH Zurich,Institut de Pharmacologie et de Biologie Structurale
[10] Boston Children’s Hospital and Harvard Medical School,undefined
[11] Université de Toulouse CNRS,undefined
[12] UPS,undefined
来源
Nature Microbiology | 2019年 / 4卷
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摘要
The early phase of influenza infection occurs in the upper respiratory tract and the trachea, but little is known about the initial events of virus recognition and control of viral dissemination by the immune system. Here, we report that inflammatory dendritic cells (IDCs) are recruited to the trachea shortly after influenza infection through type I interferon-mediated production of the chemokine CCL2. We further show that recruited IDCs express the C-type lectin receptor SIGN-R1, which mediates direct recognition of the virus by interacting with N-linked glycans present in glycoproteins of the virion envelope. Activation of IDCs via SIGN-R1 triggers the production of the chemokines CCL5, CXCL9 and CXCL10, which initiate the recruitment of protective natural killer (NK) cells in the infected trachea. In the absence of SIGN-R1, the recruitment and activation of NK cells is impaired, leading to uncontrolled viral proliferation. In sum, our results provide insight into the orchestration of the early cellular and molecular events involved in immune protection against influenza.
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页码:1930 / 1940
页数:10
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